Bone Function And Repair

Question 1

What are the functions of bone?

Answer 1

Mechanical=protect tissue + organs, provide framework for body shape, form basis of levers involved in movement

Synthetic=heamopoiesis (hold and protect red bone marrow)

Metabolic=mineral storage, fat storage (yellow marrow), acid-base Homeostasis (absorb/release alkaline salts)

Question 2

What is endochondral ossification?

Answer 2

Formation of long bones from a cartilage template. So tinted lengthening is by ossification at Epiphyseal plates (appositional growth at edges)

Question 3

What is inter-membranous ossification?

Answer 3

The formation of bone from cluster of MSC in the centre of bone-trabecular bone

(Interstitial growth in middle of bone)

Also contributes to thickening of the bone at periosteal edges in appositional growth

Question 4

How do long bones develop?

Answer 4

They require a cartilage template in order to develop by endochondral ossification

(Continued lengthening by ossification at epiphyseal plates)

Question 5

How do flat bones develop?

Skull, scapula, rib, mandible etc

Answer 5

Develop directly from Mesenchymal tissue, by intra-membranous ossification.

(Formation of bone from clusters of MSC in centre of bone)

Question 6

How does intramembranous ossification work? Using parietal bone as example.

Answer 6

Mineral deposits within the many trabecular radiate outward from a central point, this is the early primary ossification centre.

Question 7

What happens to a bony spicule once its first formed by ossification?

Answer 7

Once bony spicule has formed, then osteoblasts, osteocytes and osteoclasts remodelling it in the same way regardless if which method of ossification was used initially

Question 8

Where does intramembranous ossification take place?

Answer 8

Within the condensations of Mesenchymal tissue and not by replacing pre-existing hyaline cartilage templates.

Question 9

What is appositional growth?

Answer 9

Growth from the edges of bone, pushes cartilage at edge up and away.

Question 10

What is inter membranous growth?

Answer 10

Growth directly from Mesenchymal cells, from the middle of the bone outwards.

Question 11

What are the stages of intramembranous ossification?

Answer 11

1) Mesenchymal stem cells (MSC) form a tight cluster
2) The MSC’s transform into osteoprogenitor cells and then transform into osteoblasts
3) Osteoblats lay down an osteoid (ECM containing type 1 collagen)
4) The osteoid mineralises to form rudimentary bone tissue spicules
5) The spicules join to form trabeculae, which merge to woven bone
6) Trabeculae replaced by the lamella of mature compact bone

Question 12

What does the HAversian canal in mature bone contain? Where is it located?

Answer 12

Blood vessels, lymph vessel and neurones

Located in the osteon of the cell

Question 13

What’s the difference in arrangement between immature and mature bone?

Answer 13

Immature has osteocytes in random arrangents

Mature has osteocytes ranged in lamellae of osteons

Resorption canals in mature bone run parrelel to the osteon’s long axes

Question 14

What is cancellous bone?

Answer 14

Forms a network of fine bony columns/ plates to combine strength with lightness. The spaces are filled with bone marrow.

Question 15

What is compact bone?

Answer 15

Forms the external surfaces of bones and comprises 80% of skeletalm ass

Question 16

What is the difference between the structure of compact and cancellous bone?

Answer 16

Compact-has Haversian (verticals) canals and Volkmann’s (horizontal) canals which carry blood vessels, lymph vessels and nerves. Has circular Osteons with interstitial lamella (circular layers)

Cancellous-concentric rings of osteocytes, collagen fibres laid in lines following gravity. No canals, this provides more room for bone marrow. The canals aren’t needed as the bone cels are surrounded by marrow/fat so receive their nutrients etc this way.

Question 17

What features allow bone to resist fractures?

Answer 17

They have great tensile and compressive strength, also a degree of flexibility.
The main force lines are through the cortical bone, down the length as the body weight goes this way.

Question 18

What feature gives the bones the strength/compressibility/flexibility to resist fracture?

Answer 18

The lamella (layers) are though to be able to slip relative to each other to resist fracture. Only excessive load or an unusual direction causes fracture.

Question 19

How is bone thickened and remodelled?

Answer 19

Osteons remodel themselves to thicken bone, they mainly rethicken along the force lines as this is where additional strength is needed.

Question 20

Why does exercise effect bone strength?

Answer 20

As it constantly changes the force lines, the bone is constantly remodelled to add strength along more and more places, it increases the Osteon activity.

Inactivity increases bone resorption (1/3 lost when immobile). This is because the force lines don’t change so no new bone I layer down

Question 21

What factors in the bone itself effect bone stability?

Answer 21

Activity of osteocytes (Osteoid recycling)-can act as osteoblasts and lay down scavenged Osteoid into lamella. Or act as osteoclasts and degrade bone a little.

Activity of Osteoblasts (bone deposition)-stimulated by calcitonin, GH, oestrogen,testosterone, thyroid hormones and Vitamin A.

Activity of Osteoclasts (bone resorption)- Increased by PTH (releases Ca+ into blood), Calcitonin blocks PTH at its receptor.

Question 22

How does nutrition effect bone stability?

Answer 22

Vitamin D3 (absorbed from gut or synth by skin)-produces calcitrol for Ca2 absorption.

Vitamin C- synthesis of collagen

Vitamin K and B12- synthesis of bone proteins

Question 23

Give an brief overview of fracture repair steps.

Answer 23

1) Heamatoma formed + granulation arises
2) Procallus of granulation tissue replaced by fibrocartilaginous callus in which bony trabeculae develop
3) Endochondrial and intramembranous ossification giver is ti bony callous of cancellous bone
4) Cencellous bone replaced by cortical bone nail remodelling complete

Question 24

Describe step one of fracture repair (heamatoma formation).

Answer 24

Blood vessels in bone + periosteum break. A mass of clotted blood form. Bone cells at fracture edge die. Swelling and inflammation occurs (as granulocytes enter site). Phagocytose cells and osteoclasts remove dead and damaged bone tissue. Macrophages will eventually remove blood clot.

Question 25

Describe step 2 of fracture repair. (Fibrocartilaginous callus formation)

Answer 25

New blood vessel infiltrate the fracture heamatoma. A new procallus of granulation tissue develops. Fibroblasts produce collagen fibres to span the break. Others differentiate into chondroblasts that make sleeve of hyaline cartilage.

AT same time, osteoblasts invade fracture site and begin reconstruction of trabecular bone. (They come from nearby periosteum and endosteum.

Question 26

Describe step 3 of fracture repair (bony callous formation).

Answer 26

Within a week new bone trabeculea appear in the fibrocartilaginous callus. The trabeculae develop as the former fibrocartilaginous callus is converted to a hard callous of cancellous bone.

Epichondrial ossification replaces all cartilage with cancellous bone. Intramembranous ossification produces new cancellous bone in any gaps.

This continues about 2 months until very firm union formed across fracture

Question 27

Describe stage 4 of fracture repair (bone remodelling).

Answer 27

Cancellous bone beings to be remodelled into compact bone, especially n the prior cortical region.

The material building from the outside of bone and inwards toward medullary cavity is removed by osteoclasts.

Final shape of remodelled area is same as original bone as it responds to same mechanical stressors.

Question 28

What 2 stages happens in the bone remodelling stage to create new osteons

Answer 28

1) osteoclasts make a wide tunnel in the bone (cutting cone)
2) Ostoeblasts make a smaller tunnel or cortical bone (closing cone)

Forms new osteons (circular layers)

Question 29

What is Oteogenesis Imperfecta?

Answer 29

A mutation in COL1A gene
Incorrect production of collagen 1 fibres (they have no alpha helix so the protein bends)
This causes weak bones and increased fracture risk
Short height and stature and blue sclera
Mainly effects neonates and children (usually as they don’t live to adulthood)

Question 30

What is rickets?

Answer 30

Mainly effects children 
Vitamin D deficiency 
Poor calcium mobilisation 
Ineffective mineralisation 
Weakened bone development 
Soft bones
Short height and structure 
Painful to walk 
Characteristic bowed legs (too soft 4 weight bearing)

Question 31

What is Osteomalacia?

Answer 31

Adults “rickets”
VItamin D deficiency - lower mineralisation + increase Osteoid
Increased calcium resorption

Caused by:
Kidney disease (NO VIT D activates)
No sunlight (no VIT D synth)
Surgery on stomach/intestine (no VIT D absorbed)
Drugs (phenytoin prevents VIT D absorption)

Question 32

What are the 2 types of PRIMARY Osteoporosis?

Answer 32

Type 1- occurs in post menopause women, due to increased osteoblasts number, loss of oestrogen.

Type 2- occurs in older people (both genders), due to loss of osteoblasts function (senile osteoporosis), loss of both oestrogen and androgens.

Question 33

What is SECONDARY Osteoporosis?

Answer 33

Due to:

Drug therapy (corticosteroids)

Processes effecting bone remodelling (malnutrition, prolonged immobilisation or weightlessness)

Metabolic bone disease (hyperparathyridism (tumour), metastatic cancers)

Question 34

What is Osteoporosis?

Answer 34

When aging result in incomplete filling of osteoclast resorption bays (leaving dips and holes in bone)

Ie loss of bone tissue in veritable bodies

Question 35

What are some modifiable risk factors for Osteoporosis?

Answer 35

Calcium intake-if insufficient more likely to suffer (700mg/day for post menopause)

Exercise-immobilisation leadsto accelerated bone loss. Activity needed to maintain bone mass. Astronauts often get Osteoporosis.

Cigarette smoking in women is correlated with incidence of osteoporosis.

Question 36

What is Achondroplasia?>

Answer 36

Inherited mutation in FGF3 receptor gene
FGF promotes college formation from cartilage ( endochondral ossification affected, intramembranous ossification unaffected)

Short stature but normal head and torso as long bones cannot lengthen properly